Source of extracellular brain adenosine during hypoxia in fetal sheep.
Microdialysis was performed to determine whether hypoxia increases fetal brain adenosine (ADO) concentration through dephosphorylation of extracellular 5'-adenosine monophosphate (5-AMP). Hypoxia (fetal PaO2 approximately 14 Torr) increased fetal brain ADO levels approximately two-fold when the probes were perfused with synthetic cerebrospinal fluid (CSF) containing inhibitors of the nucleoside transporter but not with this solution plus a blocker of ecto-5'-nucleotidase (AOPCP). The hypoxia-induced rise in fetal brain ADO concentrations depends critically upon the hydrolysis of extracellular 5'-AMP.
Koos
B J
BJ
Department of Obstetrics and Gynecology, Brain Research Institute, UCLA School of Medicine, Los Angeles, CA 90095-1740, USA.
Kruger
L
L
Murray
T F
TF
D000244:Adenosine Diphosphate / Q000031:analogs & derivatives / Q000037:antagonists & inhibitors / Q000378:metabolism; D000249:Adenosine Monophosphate / Q000378:metabolism*; D000818:Animals; D002555:Cerebrospinal Fluid; D004791:Enzyme Inhibitors / Q000378:metabolism; D005260:Female; D005311:Fetal Hypoxia / Q000378:metabolism*; D017551:Microdialysis; D011247:Pregnancy; D012119:Respiration / Q000502:physiology*; D012756:Sheep; D013788:Thalamus / Q000737:chemistry / Q000201:enzymology
D004791:Enzyme Inhibitors; C523965:alpha,beta-methyleneadenosine 5'-diphosphate; D000249:Adenosine Monophosphate; D000244:Adenosine Diphosphate